JASN:唑来膦酸预防肾移植术后第一年骨丢失的疗效

2019-01-04 xing.T MedSci原创

由此可见,目前的免疫抑制方案不会导致移植后中心骨骼骨小梁丢失,唑来膦酸盐不会诱发ABD。由于移植受者的骨折最常见于外周骨折,因此临床医生应考虑在KTx时有这些部位存在骨量显著降低证据的高骨折风险患者中使用双膦酸盐治疗。

骨和矿物质疾病经常影响着肾移植(KTx)受者,并且与较高的骨折风险相关。双膦酸盐可预防或治疗此类患者的骨质流失,但有人担心这些药物可能诱发动力性骨病(ABD)。

近日,肾脏病领域权威杂志Journal of the American Society of Nephrology上发表一篇研究文章。在一项开放标签的随机试验中评估唑来膦酸盐在肾移植后第一年预防骨质流失的安全性和有效性。研究人员在受试者移植前将34名患者随机分配了接受唑来膦酸盐治疗或不治疗。研究人员使用双能X线骨密度仪(DXA)、高分辨率外周定量计算机断层扫描(HR-pQCT)和骨活检来评估32例可评估参与者在KTx移植时和移植后12个月之间的骨骼变化情况。

两组患者在KTx后骨更新均减少,但接受唑来膦酸盐治疗本身并未影响该结果。与以前的研究不同,DXA显示两组均未发生移植后骨丢失;相反,研究人员观察到腰椎和全髋部位的骨密度增加,而唑来膦酸盐具有显著的积极作用。然而,骨活组织检查显示移植后小梁连接受损(并且没有受益于唑来膦酸盐); HR-pQCT检测到外周骨骼的骨小梁丢失,其可被唑来膦酸盐部分减弱。

由此可见,目前的免疫抑制方案不会导致移植后中心骨骼骨小梁丢失,唑来膦酸盐不会诱发ABD。由于移植受者的骨折最常见于外周骨折,因此临床医生应考虑在KTx时有这些部位存在骨量显著降低证据的高骨折风险患者中使用双膦酸盐治疗。

原始出处:

Igor Denizarde Bacelar Marques,et al.A Randomized Trial of Zoledronic Acid to Prevent Bone Loss in the First Year after Kidney Transplantation.JASN,2019. https://jasn.asnjournals.org/content/early/2019/01/02/ASN.2018060656

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    2019-11-24 cy0324
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    2019-06-03 chenhongpeng
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    2019-01-06 orangesking

    0

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    2019-01-05 内科新手

    谢谢梅斯提供这么好的信息,学到很多

    0

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    2019-01-05 smartxiuxiu

    有用

    0

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    2019-01-04 医者仁心5538

    学习了

    0

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J Bone Miner Res:唑来膦酸治疗佩吉特氏病患者的希望?

最近几十年来,佩吉特氏病患者有显着较高年龄表现症状和不广泛骨骼受累的长期趋势。相似的时间框架内,有更有效的具有较长作用时间的双膦酸盐类药物被开发出来,增加了许多一生只需要一次治疗患者的希望。2017年4月,《J Bone Miner Res.》的研究调查了该病患者中,唑来膦酸治疗的应答持续时间和竞争性死亡率。

Mayo Clin Proc:多学科讨论:IV双膦酸盐颌骨坏死与骨质疏松骨折 哪个危害更大?

每年一次唑来膦酸可使骨密度降低妇女脊椎骨折减少70%和髋部骨折减少41%。然而在过去的十年中,因为担心毒性反应静脉注射(IV)和口服双膦酸盐用于骨质疏松症大幅下降,其中颌骨坏死最引人关注。2017年1月,发表在《Mayo Clin Proc》的一项研究对癌症患者和无癌症患者IV双膦酸盐后颌骨骨坏死的风险进行了比较。

Lancet oncol:狄诺塞麦对比唑来膦酸治疗新确诊的多发性骨髓瘤患者的骨骼症状的效果对比

多发性骨髓瘤的特点是产生单克隆的副蛋白和溶骨性病变,常导致骨骼相关的症状(脊髓受压,病理性骨折,或手术或放射治疗影响骨)。狄诺塞麦(denosumab),一种靶向RANKL的单克隆抗体,可减轻晚期实体肿瘤患者骨溶解或骨转移相关的骨症状。本研究旨在评估狄诺塞麦与唑来膦酸相比,用于新确诊的多发性骨髓瘤患者预防其骨骼相关症状的效果和安全性。在多个国家的多个中心开展一国际性的双盲双模拟的随机化活性对照的3

Arch of Toxicol:清华陈立功组报道临床重要药物引起肾毒性的作用机制

唑来膦酸是第三代双膦酸盐类药物,主要通过抑制破骨细胞的活性和诱导破骨细胞凋亡来抑制骨吸收,是临床上治疗恶性高钙血症、绝经后骨质疏松、控制恶性肿瘤骨转移的重要药物,具有显着的疗效。唑来膦酸临床上常见的毒副作用为肾脏损害,尤其是肾小管损害。目前,关于唑来膦酸引起肾毒性的报道大多是其引起肾毒性的临床案例,而对其导致肾毒性的分子机制报道较少。